Home Metabolism Carbohydrate Metabolism modulator 2-DG (2-Deoxy-D-glucose)

연구용

2-DG (2-Deoxy-D-glucose) Glycolysis inhibitor

제품 번호: S4701

2-DG (2-Deoxy-D-glucose), an analog of glucose, is a glycolytic inhibitor with antiviral activity. 2-Deoxy-D-glucose induces apoptosis and inhibits Herpes Simplex Virus type-1 (HSV-1) receptor expression.
2-DG (2-Deoxy-D-glucose) Carbohydrate Metabolism modulator Chemical Structure

화학 구조

분자량: 164.16

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품질 관리 (Quality Control)

배치: 순도: >97%
97

화학 정보, 보관 및 안정성 (Chemical Information, Storage & Stability)

분자량 164.16 화학식

C6H12O5

 보관 (수령일로부터)
CAS 번호 154-17-6 SDF 다운로드 원액 보관

동의어 2-deoxyglucose, NSC 15193, 2-Deoxy-D-arabino-hexose, D-Arabino-2-deoxyhexose Smiles C(C=O)C(C(C(CO)O)O)O

용해도 (Solubility)

In vitro
배치:

DMSO : 500 mg/mL (3045.8 mM) 50°C 수조에서 가온; 초음파 처리;
(수분으로 오염된 DMSO는 용해도를 감소시킬 수 있습니다. 신선하고 무수 DMSO를 사용하십시오.)

Water : 83 mg/mL

Ethanol : 8 mg/mL

몰농도 계산기

질량 농도 부피 분자량
희석 계산기 분자량 계산기

In vivo
배치:

생체 내 제형 계산기 (투명한 용액)

1단계: 아래 정보 입력 (권장: 실험 중 손실을 고려하여 추가 동물 포함)

mg/kg g μL

2단계: 생체 내 제형 입력 (이것은 계산기일 뿐 제형이 아닙니다. 용해도 섹션에 생체 내 제형이 없는 경우 먼저 당사에 문의하십시오.)

% DMSO % % Tween 80 % ddH2O
%DMSO %

계산 결과:

작업 농도: mg/ml;

DMSO 원액 준비 방법: mg 약물 사전 용해 μL DMSO ( 원액 농도 mg/mL, 농도가 해당 약물 배치의 DMSO 용해도를 초과하는 경우 먼저 당사에 문의하십시오. )

생체 내 제형 준비 방법: 취하다 μL DMSO 원액, 다음 추가μL PEG300, 혼합하고 투명하게 한 다음 추가μL Tween 80, 혼합하고 투명하게 한 다음 추가 μL ddH2O, 혼합하고 투명하게 합니다.

생체 내 제형 준비 방법: 취하다 μL DMSO 원액, 다음 추가 μL 옥수수 기름, 혼합하고 투명하게 합니다.

참고: 1. 다음 용매를 추가하기 전에 액체가 투명한지 확인하십시오.
2. 용매를 순서대로 추가해야 합니다. 다음 용매를 추가하기 전에 이전 추가에서 얻은 용액이 투명한 용액인지 확인해야 합니다. 와동, 초음파 또는 뜨거운 물 중탕과 같은 물리적 방법을 사용하여 용해를 도울 수 있습니다.

작용 메커니즘 (Mechanism of Action)

Targets/IC50/Ki
glycolysis
시험관 내(In vitro)
2-Deoxy-D-glucose (2-DG) activates AKT function through phosphatidylinositol 3-kinase (PI3K) and is independent of glycolysis or mTOR inhibition. Its treatments disrupt the binding between insulin-like growth factor 1 (IGF-1) and IGF-binding protein 3 (IGFBP3) so that the free form of IGF-1 could be released from the IGF-1·IGFBP3 complex to activate IGF-1 receptor (IGF1R) signaling. 2-DG-induced activation of many survival pathways can be jointly attenuated through IGF1R inhibition. This compound also induces time- and dose-dependent ERK phosphorylation. It is readily transported into cells and is phosphorylated by hexokinase, but cannot be metabolized further and accumulates in the cell. This leads to ATP depletion and the induction of cell-death. 2DG significantly suppresses proliferation, causes apoptosis and reduces migration of murine endothelial cells, inhibiting formation of lamellipodia and filopodia and causing disorganization of F-actin filaments in murine endothelial cell.
생체 내(In vivo)
Treatment of cancer patients with relatively high doses of 2-Deoxy-D-glucose (2-DG) (greater than 200 mg/kg) was largely ineffective in managing tumor growth. Side effects of this compound included elevated blood glucose levels, progressive weight loss with lethargy, and behavioral symptoms of hypoglycemia. It enhances isoflurane-induced loss of righting reflex in mice. By reducing metabolism, 2-DG treatment can decrease body temperature in rodent, enhancing sensitivity to anesthetics. A diet containing it significantly increased serum ketone body level and brain expression of enzymes required for ketone body metabolism. The 2-DG-induced maintenance of mitochondrial bioenergetics was paralleled by simultaneous reduction in oxidative stress. Further, treated mice exhibited a significant reduction of both amyloid precursor protein (APP) and amyloid beta (Aβ) oligomers, which was paralleled by significantly increased α-secretase and decreased γ-secretase expression, indicating that this compound induced a shift towards a non-amyloidogenic pathway. It increased expression of genes involved in Aβ clearance pathways, degradation, sequestering, and transport. Concomitant with increased bioenergetic capacity and reduced β-amyloid burden, 2-DG significantly increased expression of neurotrophic growth factors, BDNF and NGF, thus reduces pathology in female mouse model of Alzheimer's disease.
참조
  • [4] https://pubmed.ncbi.nlm.nih.gov/21747957/
  • [5] https://pubmed.ncbi.nlm.nih.gov/26398947/

임상시험 정보 (Clinical Trial Information)

(데이터 출처 https://clinicaltrials.gov, 업데이트 날짜 2024-05-22)

NCT 번호 모집 조건 스폰서/협력자 시작일 단계
NCT02558140 Completed
Neoplasms
Hoffmann-La Roche
 October 11 2015 Phase 1
NCT01998841 Completed
Alzheimer''s Disease
Genentech Inc.|Banner Alzheimer''s Institute|National Institute on Aging (NIA)
 December 20 2013 Phase 2